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We previously reported that renal\u2010selective depletion and germline deletion of\n              <jats:italic>\n                <jats:styled-content style=\"fixed-case\">DJ<\/jats:styled-content>\n                \u20101\n              <\/jats:italic>\n              increases blood pressure in mice. This study aimed to determine the mechanisms involved in the oxidative stress\u2013mediated hypertension in\n              <jats:italic>\n                <jats:styled-content style=\"fixed-case\">DJ<\/jats:styled-content>\n                \u20101\n              <\/jats:italic>\n              <jats:sup>\n                <jats:italic>\u2212\/\u2212<\/jats:italic>\n              <\/jats:sup>\n              mice.\n            <\/jats:p>\n          <\/jats:sec>\n          <jats:sec xml:lang=\"en\">\n            <jats:title>Methods and Results<\/jats:title>\n            <jats:p xml:lang=\"en\">\n              There were no differences in sodium excretion, renal renin expression, renal\n              <jats:styled-content style=\"fixed-case\">NADPH<\/jats:styled-content>\n              oxidase activity, and serum creatinine levels between\n              <jats:italic>\n                <jats:styled-content style=\"fixed-case\">DJ<\/jats:styled-content>\n                \u20101\n              <\/jats:italic>\n              <jats:sup>\n                <jats:italic>\u2212\/\u2212<\/jats:italic>\n              <\/jats:sup>\n              and wild\u2010type mice. Renal expression of nitro\u2010tyrosine, malondialdehyde, and urinary kidney injury marker\u20101 were increased in\n              <jats:italic>\n                <jats:styled-content style=\"fixed-case\">DJ<\/jats:styled-content>\n                \u20101\n              <\/jats:italic>\n              <jats:sup>\n                <jats:italic>\u2212\/\u2212<\/jats:italic>\n              <\/jats:sup>\n              mice relative to wild\u2010type littermates.\n              <jats:styled-content style=\"fixed-case\">mRNA<\/jats:styled-content>\n              expression of mitochondrial heat shock protein 60 was also elevated in kidneys from\n              <jats:italic>\n                <jats:styled-content style=\"fixed-case\">DJ<\/jats:styled-content>\n                \u20101\n              <\/jats:italic>\n              <jats:sup>\n                <jats:italic>\u2212\/\u2212<\/jats:italic>\n              <\/jats:sup>\n              mice, indicating the presence of oxidative stress. Tempol\u2010treated\n              <jats:italic>\n                <jats:styled-content style=\"fixed-case\">DJ<\/jats:styled-content>\n                \u20101\n              <\/jats:italic>\n              <jats:sup>\n                <jats:italic>\u2212\/\u2212<\/jats:italic>\n              <\/jats:sup>\n              mice presented higher serum nitrite\/nitrate levels than vehicle\u2010treated\n              <jats:italic>\n                <jats:styled-content style=\"fixed-case\">DJ<\/jats:styled-content>\n                \u20101\n              <\/jats:italic>\n              <jats:sup>\n                <jats:italic>\u2212\/\u2212<\/jats:italic>\n              <\/jats:sup>\n              mice, suggesting a role of the\n              <jats:styled-content style=\"fixed-case\">NO<\/jats:styled-content>\n              system in the high blood pressure of this model. Tempol treatment normalized renal kidney injury marker\u20101 and malondialdehyde expression as well as blood pressure in\n              <jats:italic>\n                <jats:styled-content style=\"fixed-case\">DJ<\/jats:styled-content>\n                \u20101\n              <\/jats:italic>\n              <jats:sup>\n                <jats:italic>\u2212\/\u2212<\/jats:italic>\n              <\/jats:sup>\n              mice, but had no effect in wild\u2010type mice. The renal\n              <jats:italic>Ucp2<\/jats:italic>\n              <jats:styled-content style=\"fixed-case\">mRNA<\/jats:styled-content>\n              expression was increased in\n              <jats:italic>\n                <jats:styled-content style=\"fixed-case\">DJ<\/jats:styled-content>\n                \u20101\n              <\/jats:italic>\n              <jats:sup>\n                <jats:italic>\u2212\/\u2212<\/jats:italic>\n              <\/jats:sup>\n              mice versus wild\u2010type and was also normalized by tempol. The renal\u2010selective silencing of\n              <jats:italic>Ucp2<\/jats:italic>\n              led to normalization of blood pressure and serum nitrite\/nitrate ratio in\n              <jats:italic>\n                <jats:styled-content style=\"fixed-case\">DJ<\/jats:styled-content>\n                \u20101\n              <\/jats:italic>\n              <jats:sup>\n                <jats:italic>\u2212\/\u2212<\/jats:italic>\n              <\/jats:sup>\n              mice.\n            <\/jats:p>\n          <\/jats:sec>\n          <jats:sec xml:lang=\"en\">\n            <jats:title>Conclusions<\/jats:title>\n            <jats:p xml:lang=\"en\">\n              The deletion of\n              <jats:italic>\n                <jats:styled-content style=\"fixed-case\">DJ<\/jats:styled-content>\n                \u20101\n              <\/jats:italic>\n              leads to oxidative stress\u2013induced hypertension associated with downregulation of\n              <jats:styled-content style=\"fixed-case\">NO<\/jats:styled-content>\n              function, and overexpression of\n              <jats:italic>Ucp2<\/jats:italic>\n              in the kidney increases blood pressure in\n              <jats:italic>\n                <jats:styled-content style=\"fixed-case\">DJ<\/jats:styled-content>\n                \u20101\n              <\/jats:italic>\n              <jats:sup>\n                <jats:italic>\u2212\/\u2212<\/jats:italic>\n              <\/jats:sup>\n              mice. To our knowledge, this is the first report providing evidence of the role of uncoupling protein 2 in blood pressure regulation.\n            <\/jats:p>\n          <\/jats:sec>","DOI":"10.1161\/jaha.118.011856","type":"journal-article","created":{"date-parts":[[2019,4,18]],"date-time":"2019-04-18T09:04:28Z","timestamp":1555578268000},"update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":13,"title":["Uncoupling Protein 2 Increases Blood Pressure in DJ\u20101 Knockout Mice"],"prefix":"10.1161","volume":"8","author":[{"given":"Carmen","family":"De Miguel","sequence":"first","affiliation":[{"name":"Section\u00a0of Cardio\u2010Renal Physiology and Medicine Division of Nephrology Department of Medicine University of Alabama at Birmingham AL"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"William C.","family":"Hamrick","sequence":"additional","affiliation":[{"name":"Section\u00a0of Cardio\u2010Renal Physiology and Medicine Division of Nephrology Department of Medicine University of Alabama at Birmingham AL"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Randee","family":"Sedaka","sequence":"additional","affiliation":[{"name":"Section\u00a0of Cardio\u2010Renal Physiology and Medicine Division of Nephrology Department of Medicine University of Alabama at Birmingham AL"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Sudha","family":"Jagarlamudi","sequence":"additional","affiliation":[{"name":"Division of Renal Diseases &amp; Hypertension Department of Medicine The George Washington University School of Medicine and Health Sciences Washington DC"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Laureano D.","family":"Asico","sequence":"additional","affiliation":[{"name":"Division of Renal Diseases &amp; Hypertension Department of Medicine The George Washington University School of Medicine and Health Sciences Washington DC"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Pedro A.","family":"Jose","sequence":"additional","affiliation":[{"name":"Division of Renal Diseases &amp; Hypertension Department of Medicine The George Washington University School of Medicine and Health Sciences Washington DC"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Santiago","family":"Cuevas","sequence":"additional","affiliation":[{"name":"Research Center for Genetic Medicine Children's National Health System Washington DC"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"276","reference":[{"key":"e_1_3_1_2_2","doi-asserted-by":"publisher","DOI":"10.1136\/heartjnl-2016-310794"},{"key":"e_1_3_1_3_2","doi-asserted-by":"publisher","DOI":"10.1089\/ars.2013.5259"},{"key":"e_1_3_1_4_2","doi-asserted-by":"publisher","DOI":"10.1111\/j.1471-4159.2008.05333.x"},{"key":"e_1_3_1_5_2","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M507124200"},{"key":"e_1_3_1_6_2","doi-asserted-by":"publisher","DOI":"10.1006\/bbrc.1997.6132"},{"key":"e_1_3_1_7_2","doi-asserted-by":"publisher","DOI":"10.1002\/jnr.21831"},{"key":"e_1_3_1_8_2","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.0000254486.00883.3d"},{"key":"e_1_3_1_9_2","doi-asserted-by":"publisher","DOI":"10.3390\/ijms140917553"},{"key":"e_1_3_1_10_2","doi-asserted-by":"publisher","DOI":"10.1161\/hypertensionaha.111.185744"},{"key":"e_1_3_1_11_2","doi-asserted-by":"publisher","DOI":"10.1161\/HYPERTENSIONAHA.114.04525"},{"key":"e_1_3_1_12_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.mito.2017.03.005"},{"key":"e_1_3_1_13_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.bcp.2016.05.004"},{"key":"e_1_3_1_14_2","first-page":"2493","article-title":"Effect of uncoupling protein 2 on high\u2010glucose induced mitochondrial damage and apoptosis of cardiomyocytes","volume":"96","author":"Diao JY","year":"2016","unstructured":"Diao JY, Wei J, Yan R, Lin L, Li H. 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